Development Of Joint Destruction Research Articles

Into the bag of knowledge and experience of a doctor of general practice. Juvenile rheumatoid arthritis in a 6-year-old boy: clinic, diagnosis, treatment

Juvenile idiopathic arthritis is one of the most common rheumatic diseases of childhood, leading to disability. This is a multifactorial polygenic disease with an aggressive course, the development of joint destruction and visceral disorders. This article presents a clinical case dedicated to juvenile idiopathic arthritis with systemic onset. The features of the course and treatment of the disease, the effectiveness of therapy prescribed in accordance with clinical recommendations are noted.

Psoriatic arthritis. Clinical guidelines for diagnosis and treatment

In recent years, there has been a considerable rise in the incidence of psoriatic arthritis (PsA) and an increase in the number of cases of its severe course, which leads to the marked deterioration of quality of life (QL), to disability and early disability. PsA is characterized by its chronic progressive course, the development of joint destruction and ankylosis, multiple intra-articular osteolysis, spondylitis and frequently accompanied by various comorbidities. The important aspects of the prevention of joint functional disorders and erosion and their successful therapy are early diagnosis of PsA in patients with psoriasis (Ps) and timely consultation with a rheumatologist. The early use of pathogenetically sound therapy for PsA reduces the likelihood of irreversible damage to the joints, spine, and viscera in these patients. The main goal of PsA pharmacotherapy is to achieve remission or minimal activity of a disease (arthritis, spondylitis, enthesitis, dactylitis, and Ps), to slow or prevent radiological progression, to increase life expectancy, to improve QL for patients, and to lower the risk of comorbidities. These guidelines have been worked out jointly by rheumatologists and dermatovenereologists in order to improve the diagnosis of PsA in patients with Ps and to timely initiate adequate therapy.

Relationship between Synovial Fluid Inflammatory Cells and Grade of Inflammation of Synovium in Patients with Spondylarthropathy

Objective To study whether the analysis of synovial fluid (SF) inflammatory cells can be used for the estimation of the grade of inflammation in the synovium and, therefore, for the prediction of the possible development of joint destruction in spondylarthropathy. Methods Forty-one patients with spondylarthropathy and hydropsy in a knee joint were studied. The cellular composition of SF aspirates was investigated and the grade of inflammation in synovial biopsy samples was evaluated by analyzing histological needle biopsy specimens. Results The count of SF polymorphonuclear leukocytes (PMN) reflected significantly the activity of acute inflammation. None of the SF cells reflected the chronic inflammation in the synovium. Conclusion The number of SF PMNs may reflect the severity of acute inflammatory process in the synovium in patients with spodylarthropathy at a given moment, but the analysis of SF aspirates may not be of use in estimating the activity of chronic phase of inflammation presumably causing the joint destruction.

Haemophilic synovitis: basic concepts

Chronic synovitis is a serious complication of haemophilia that should be understood to avoid or minimize its consequences (articular damage and joint degeneration). Haematological prophylaxis and treatment are paramount during the life of people with haemophilia. However, as about 80% of bleedings in haemophilia affect the musculo-skeletal system, the role of orthopaedic surgeons, rehabilitation physicians and physiotherapists is very important in the context of the multidisciplinary team. Synovitis can firstly be prevented and/or controlled with medical treatment and then be treated by synoviorthesis or surgical synovectomy. In this article, the author reviews some current basic principles on the prevention and treatment of haemophilic synovitis to avoid further development of joint destruction (haemophilic arthropathy).

Infliximab acts directly on human osteoclast precursors and enhances osteoclast formation induced by receptor activator of nuclear factor κB ligand in vitro

Infliximab is known to protect against the development of joint destruction. In the present study, we sought to determine whether Infliximab acts directly on human osteoclast precursors and influences monocyte-osteoclast differentiation induced by receptor activator of nuclear factor kappaB ligand (RANKL) in vitro. Peripheral blood mononuclear cells (PBMCs) isolated from rheumatoid arthritis (RA) patients and normal controls were cultured in the presence of RANKL and macrophage colony stimulating factor. Infliximab, antihuman tumor necrosis factor alpha (TNFalpha), antihuman TNF soluble receptor p55 (TNFR p55), and antihuman TNF soluble receptor p75 (TNFR p75) antibodies were added. Osteoclast formation was determined by assessing the number of tartrate-resistant acid phosphatase (TRAP) staining cells and the extent of lacunar resorption. Addition of Infliximab resulted in a marked increase in the number of TRAP-positive multinucleated cells (TRAP(+) MNCs) and in the extent of lacunar resorption compared with the control cultures. Antihuman TNFalpha antibody showed the same effect; however, the addition of neither TNFR p55 nor TNFR p75 antibody affected the extent of TRAP(+) MNCs and lacunar resorption. Our results suggest that infliximab acts directly on early osteoclast precursors, and stimulates osteoclast formation and lacunar resorption induced by RANKL in vitro.

Infliximab acts directly on human osteoclast precursors and enhances osteoclast formation induced by receptor activator of nuclear factor κB ligand in vitro

Infliximab is known to protect against the development of joint destruction. In the present study, we sought to determine whether Infliximab acts directly on human osteoclast precursors and influences monocyte-osteoclast differentiation induced by receptor activator of nuclear factor κB ligand (RANKL) in vitro. Peripheral blood mononuclear cells (PBMCs) isolated from rheumatoid arthritis (RA) patients and normal controls were cultured in the presence of RANKL and macrophage colony stimulating factor. Infliximab, antihuman tumor necrosis factor α (TNFα), antihuman TNF soluble receptor p55 (TNFR p55), and antihuman TNF soluble receptor p75 (TNFR p75) antibodies were added. Osteoclast formation was determined by assessing the number of tartrate-resistant acid phosphatase (TRAP) staining cells and the extent of lacunar resorption. Addition of Infliximab resulted in a marked increase in the number of TRAP-positive multinucleated cells (TRAP+ MNCs) and in the extent of lacunar resorption compared with the control cultures. Antihuman TNFα antibody showed the same effect; however, the addition of neither TNFR p55 nor TNFR p75 antibody affected the extent of TRAP+ MNCs and lacunar resorption. Our results suggest that infliximab acts directly on early osteoclast precursors, and stimulates osteoclast formation and lacunar resorption induced by RANKL in vitro.

Connective tissue markers of rheumatoid arthritis

Rheumatoid arthritis (RA) is a common systemic autoimmune disorder of unknown aetiology. The most common outcome of RA is a progressive development of joint destruction and deformity. Early introduction of disease-modifying antirheumatic drugs seems important for prevention of the long term injuries of articular cartilage and bone. Early diagnosis and selection of patients with rapidly progressive disease therefore is of clinical significance. Routine laboratory tests are valuable in monitoring for renal, hepatic and haematological side effects of medical treatment. Determination of rheumatoid factor contributes to the classification of arthritis as RA, and acute phase reactants are useful for quantifying and comparing the level of inflammatory activity in the course of a given patient. There is, however, a lack of sensitive and specific biochemical markers for RA, and frontline biochemical research is devoted to characterizing molecules which are of diagnostic and prognostic value, as well as molecules which are indicators of the degree of joint cartilage and bone destruction. The present survey summarizes current knowledge concerning possible tissue-specific marker molecules of RA.

A physically demanding occupation predicts premature retirement among patients with erosive arthritis

The aim of this study was to assess the intensity of exercise and energy expenditure of patients with recent onset inflammatory arthritis in their occupational environments and leisure time physical activities. The exercise intensities and energy expenditures of 41 early inflammatory arthritis patients and 20 matched healthy controls were assessed in occupational work and in leisure time physical activities during a 3.5-year follow-up using metabolic unit values. Disease activity was assessed by erythrocyte sedimentation rate and Ritchie's articular index. Subjective disability was assessed by the Stanford Health Assessment Questionnaire and the extent of joint damage on X-rays of the hands and feet following the method of Larsen et al (1977). Furthermore, 21 patients initially carried out progressive strength training for a 6-month period, while the rest of the subjects only maintained their daily physical activities. Our results indicate that the high physical requirements of occupational work were related to the development of joint destruction, work disability and the premature professional retirement of the inflammatory arthritis patients. The exercise intensities and energy expenditures in leisure time physical activities were lower when compared with daily work and were of minor importance. However, the 6-month strength training had a positive impact on patient outcome. Patients in physically demanding jobs who contract inflammatory arthritis need early occupational and physical rehabilitation to prevent progressive structural joint damage and premature retirement.

Prognostic indicators of joint destruction in systemic-onset juvenile rheumatoid arthritis

We retrospectively reviewed the charts and radiographs of 38 patients with systemic-onset juvenile rheumatoid arthritis, attempting to identify early in the disease course the clinical and laboratory observations most predictive of the later development of destructive arthritis. In 12 of the patients, destructive arthritis developed within 2 years of disease onset. When first examined, these patients could not readily be differentiated from those in whom joint destruction did not develop, but they more commonly had hepatosplenomegaly (p less than 0.04), serositis (p less than 0.01), and a lower mean serum albumin concentration (26.7 vs 31.3 gm/L; p less than 0.02). However, by 6 months after onset, patients with destructive arthritis more frequently had persistent systemic symptoms (92% vs 12%; p less than 0.0001), polyarthritis (67% vs 19%; p less than 0.0005), a lower mean hemoglobin level (95 vs 114 gm/L; p less than 0.001), a higher mean leukocyte count (21.2 vs 10 x 10(9)/L; p less than 0.0003), a higher mean platelet count (794 vs 400 x 10(9)/L; p less than 0.0001), and a higher mean erythrocyte sedimentation rate (43 vs 24 mm/hr; p less than 0.05). Multivariate analysis of the results at 6 months revealed that persistent systemic symptoms and a platelet count greater than or equal to 600 x 10(9)/L were the variables most highly predictive of the later development of joint destruction. We conclude that patients at high risk for the development of destructive arthritis may be identified within 6 months of disease onset, thereby indicating the need for more aggressive early therapy.